Multistage Delivery of Active Agents
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Combination of Cabazitaxel and Plicamycin Induces Cell Death in Drug Resistant B-Cell Acute Lymphoblastic Leukemia
Clinical and Translational Science Institute Centers 9-1-2018 Combination of cabazitaxel and plicamycin induces cell death in drug resistant B-cell acute lymphoblastic leukemia Rajesh R. Nair West Virginia University Debbie Piktel West Virginia University Werner J. Geldenhuys West Virginia University Laura F. Gibson West Virginia University Follow this and additional works at: https://researchrepository.wvu.edu/ctsi Part of the Medicine and Health Sciences Commons Digital Commons Citation Nair, Rajesh R.; Piktel, Debbie; Geldenhuys, Werner J.; and Gibson, Laura F., "Combination of cabazitaxel and plicamycin induces cell death in drug resistant B-cell acute lymphoblastic leukemia" (2018). Clinical and Translational Science Institute. 34. https://researchrepository.wvu.edu/ctsi/34 This Article is brought to you for free and open access by the Centers at The Research Repository @ WVU. It has been accepted for inclusion in Clinical and Translational Science Institute by an authorized administrator of The Research Repository @ WVU. For more information, please contact [email protected]. HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Leuk Res Manuscript Author . Author manuscript; Manuscript Author available in PMC 2019 September 01. Published in final edited form as: Leuk Res. 2018 September ; 72: 59–66. doi:10.1016/j.leukres.2018.08.002. Combination of cabazitaxel and plicamycin induces cell death in drug resistant B-cell acute lymphoblastic leukemia Rajesh R. Naira, Debbie Piktelb, Werner J. Geldenhuysc, -
Synthesis and Antitumor Evaluation of Novel Bis-Triaziquone Derivatives
Molecules 2009, 14, 2306-2316; doi:10.3390/molecules14072306 OPEN ACCESS molecules ISSN 1420-3049 www.mdpi.com/journal/molecules Article Synthesis and Antitumor Evaluation of Novel Bis-Triaziquone Derivatives Cheng Hua Huang 1,3, Hsien-Shou Kuo 2, Jia-Wen Liu 3 and Yuh-Ling Lin 3,* 1 Cathay General Hospital, 280 Renai Rd. Sec.4, Taipei, Taiwan 2 Department of Biochemistry, Taipei Medical University, 250 Wu-Hsin St. Taipei, Taiwan 3 College of Medicine, Fu-Jen Catholic University, 510 Chung Cheng Rd., Hsin-Chuang, Taipei Hsien 24205, Taiwan * Author to whom correspondence should be addressed; E-mail: [email protected] Received: 30 April 2009; in revised form: 19 June 2009 / Accepted: 23 June 2009 / Published: 29 June 2009 Abstract: Aziridine-containing compounds have been of interest as anticancer agents since late 1970s. The design, synthesis and study of triaziquone (TZQ) analogues with the aim of obtaining compounds with enhanced efficacy and reduced toxicity are an ongoing research effort in our group. A series of bis-type TZQ derivatives has been prepared and their cytotoxic activities were investigated. The cytotoxicity of these bis-type TZQ derivatives were tested on three cancer lines, including breast cancer (BC-M1), oral cancer (OEC-M1), larynx epidermal cancer (Hep2) and one normal skin fibroblast (SF). Most of these synthetic derivatives displayed significant cytotoxic activities against human carcinoma cell lines, but weak activities against SF. Among tested analogues the bis-type TZQ derivative 1a showed lethal effects on larynx epidermal carcinoma cells (Hep2), with an LC50 value of 2.02 M, and also weak cytotoxic activity against SF cells with an LC50 value over 10 M for 24 hr treatment. -
Methods for Predicting the Survival Time of Patients Suffering from a Lung Cancer
THETWO TORTOITUUSN 20180252720A1ULLUM HOLATIN ( 19) United States (12 ) Patent Application Publication ( 10) Pub . No. : US 2018 / 0252720 A1 DIEU -NOSJEAN et al. (43 ) Pub. Date : Sep . 6 , 2018 (54 ) METHODS FOR PREDICTING THE Publication Classification SURVIVAL TIME OF PATIENTS SUFFERING (51 ) Int . Ci. FROM A LUNG CANCER GOIN 33 /574 ( 2006 .01 ) (71 ) Applicants : INSERM (INSTITUT NATIONAL ( 52 ) U . S . CI. DE LA SANTE ET DE LA CPC .. GOIN 33 /57423 (2013 . 01) ; GOIN 2800/ 52 RECHERCHE MEDICALE ) , Paris ( 2013 . 01 ) (FR ) ; UNIVERSITE PARIS DESCARTES , Paris ( FR ) ; SORBONNE UNIVERSITE , Paris (57 ) ABSTRACT (FR ) ; UNIVERSITE PARIS DIDEROT - PARIS 7 , Paris ( FR ) ; The present invention relates to methods for predicting the ASSISTANCE survival time of patients suffering from a lung cancer . In PUBLIQUE -HOPITAUX DE PARIS particular , the present invention relates to a method for (ADHP ) , Paris (FR ) predicting the survival time of a subject suffering from a lung cancer comprising the steps of i) quantifying the ( 72 ) Inventors: Marie - Caroline DIEU - NOSJEAN , density of regulatory T ( Treg ) cells in a tumor tissue sample Paris (FR ) ; Wolf Herdman obtained from the subject, ii ) quantifying the density of one FRIDMAN , Paris ( FR ) ; Catherine further population of immune cells selected from the group SAUTES - FRIDMAN , Paris ( FR ) ; consisting of TLS -mature DC or TLS - B cells or Tconv cells , Priyanka DEVI, Paris (FR ) CD8 + T cells or CD8 + Granzyme - B + T cells in said tumor tissue sample , iii ) comparing the densities quantified at steps (21 ) Appl. No. : 15/ 754 , 640 i ) and ii ) with their corresponding predetermined reference values and iv ) concluding that the subject will have a short ( 22 ) PCT Filed : Aug . -
California Proposition 65 Toxicity List
STATE OF CALIFORNIA ENVIRONMENTAL PROTECTION AGENCY OFFICE OF ENVIRONMENTAL HEALTH HAZARD ASSESSMENT SAFE DRINKING WATER AND TOXIC ENFORCEMENT ACT OF 1986 CHEMICALS KNOWN TO THE STATE TO CAUSE CANCER OR REPRODUCTIVE TOXICITY 4-Mar-05 The Safe Drinking Water and Toxic Enforcement Act of 1986 requires that the Governor revise and Chemical Type of Toxicity CAS No. Date Listed A-alpha-C (2-Amino-9H-pyrido[2,3-b]indole) cancer 26148685 1-Jan-90 Acetaldehyde cancer 75070 1-Apr-88 Acetamide cancer 60355 1-Jan-90 Acetazolamide developmental 59665 20-Aug-99 Acetochlor cancer 34256821 1-Jan-89 Acetohydroxamic acid developmental 546883 1-Apr-90 2-Acetylaminofluorene cancer 53963 1-Jul-87 Acifluorfen cancer 62476599 1-Jan-90 Acrylamide cancer 79061 1-Jan-90 Acrylonitrile cancer 107131 1-Jul-87 Actinomycin D cancer 50760 1-Oct-89 Actinomycin D developmental 50760 1-Oct-92 Adriamycin (Doxorubicin hydrochloride) cancer 23214928 1-Jul-87 AF-2;[2-(2-furyl)-3-(5-nitro-2-furyl)]acrylamide cancer 3688537 1-Jul-87 Aflatoxins cancer --- 1-Jan-88 Alachlor cancer 15972608 1-Jan-89 Alcoholic beverages, when associated with alcohol abuse cancer --- 1-Jul-88 Aldrin cancer 309002 1-Jul-88 All-trans retinoic acid developmental 302794 1-Jan-89 Allyl chloride Delisted October 29, 1999 cancer 107051 1-Jan-90 Alprazolam developmental 28981977 1-Jul-90 Altretamine developmental, male 645056 20-Aug-99 Amantadine hydrochloride developmental 665667 27-Feb-01 Amikacin sulfate developmental 39831555 1-Jul-90 2-Aminoanthraquinone cancer 117793 1-Oct-89 p -Aminoazobenzene cancer -
PEMD-91-12BR Off-Label Drugs: Initial Results of a National Survey
11 1; -- __...._-----. ^.-- ______ -..._._ _.__ - _........ - t Ji Jo United States General Accounting Office Washington, D.C. 20648 Program Evaluation and Methodology Division B-242851 February 25,199l The Honorable Edward M. Kennedy Chairman, Committee on Labor and Human Resources United States Senate Dear Mr. Chairman: In September 1989, you asked us to conduct a study on reimbursement denials by health insurers for off-label drug use. As you know, the Food and Drug Administration designates the specific clinical indications for which a drug has been proven effective on a label insert for each approved drug, “Off-label” drug use occurs when physicians prescribe a drug for clinical indications other than those listed on the label. In response to your request, we surveyed a nationally representative sample of oncologists to determine: . the prevalence of off-label use of anticancer drugs by oncologists and how use varies by clinical, demographic, and geographic factors; l the extent to which third-party payers (for example, Medicare intermediaries, private health insurers) are denying payment for such use; and l whether the policies of third-party payers are influencing the treatment of cancer patients. We randomly selected 1,470 members of the American Society of Clinical Oncologists and sent them our survey in March 1990. The sam- pling was structured to ensure that our results would be generalizable both to the nation and to the 11 states with the largest number of oncologists. Our response rate was 56 percent, and a comparison of respondents to nonrespondents shows no noteworthy differences between the two groups. -
Human Cytogenetics Prenatal Diagnostics
Cytogenetics Human Cytogenetics Prenatal Diagnostics Optimized Medium for Culture and Genetic Analysis of Human Amniotic Fluid Cells BIOAMF-1 and Chorionic Villi ( CV ) Samples Basal Medium and Supplement Chromosome Karyotyping was first developed in the BIOAMF-1 is designed for the primary culture of field of Cytogenetics. human amniotic fluid cells and chorionic villi (CV) The basic principle of the method is the preparation samples in both open (5% CO2) and closed systems. of chromosomes for microscopic observation by The medium allows rapid growth of amniocytes or arresting cell mitosis at metaphase with colchicine and treating the cells with a hypotonic solution. This chorionic villi for use in karyotyping. is followed by regular or fluorescent staining of the No supplementation with serum or serum- chromosomes, which are then tested with the aid of a substitutes is necessary. microscope and computer programs to arrange and The medium consists of two components: basal identify the chromosomes for the presence of genetic medium and frozen supplements. abnormalities. In principle, this method enables the identification Instructions for Use of any abnormality - excess chromosomes or For the preparation of 500ml complete medium, use chromosome deficiency, broken chromosomes, 01-190-1A with 01-192-1E. or excess genetic material (as a result of a For the preparation of 100ml complete medium, use recombination process). 01-190-1B with 01-192-1D. Clinical cytogenetics laboratories use this method Thaw the BIOAMF-1 Supplement by swirling in a with amniotic fluid, chorionic villi, blood cells, skin cells, and so on, which can be cell cultured to obtain 37ºC water bath, and transfer the contents to the mitotic cells. -
The Chemotherapy of Malignant Disease -Practical and Experimental Considerations
Postgrad Med J: first published as 10.1136/pgmj.41.475.268 on 1 May 1965. Downloaded from POSTGRAD. MED. J. (1965), 41,268 THE CHEMOTHERAPY OF MALIGNANT DISEASE -PRACTICAL AND EXPERIMENTAL CONSIDERATIONS JOHN MATTHIAS, M.D., M.R.C.P., F.F.A., R.C.S. Physician, The Royal Marsden Hospital, London, S.W.3. THE TERM chemotherapy was introduced by positively charged alkyl (CH2) radicles of Ehrlich to describe the specific and effective the agent. treatment of infectious disease by chemical (a) The nitrogen mustards: mustine (HN2 substances. It is currently also applied to the 'nitrogen mustard', mechlorethamine, treatment of malignant disease. Unfortunately mustargen), trimustine (Trillekamin no aspect of tumour metabolism has been HN3), chlorambucil (Leukeran, phenyl discovered which has allowed the development butyric mustard), melphalan (Alkeran, of drugs capable of acting specifically upon the phenyl alanine mustard), uramustine malignant cell, so that cytotoxic drugs also (Uracil mustard), cyclophosphamide affect normal cells to a greater or lesser degree. (Endoxan or Cytoxan), mannomustine The most susceptible or sensitive of the normal (DegranoO). tissues are those with the highest rates of cell (b) The ethylenamines: tretamine (trie- turnover and include the haemopoietic and thanomelamine, triethylene melamine, lympho-reticular tissues, the gastro-intestinal TEM), thiotepa (triethylene thiopho- the the testis and the hair epithelium, ovary, sphoramide), triaziquone (Trenimon).by copyright. follicles. (c) The epoxides: triethyleneglycoldigly- Cancer chemotherapy may be said to encom- cidyl ether (Epodyl). pass all treatments of a chemical nature (d) The sulphonic acid esters: busulphan administered to patients with the purpose of (Myleran), mannitol myleran. restricting tumour growth or destroying tumour 2. -
Lonidamine Induces Apoptosis in Drug-Resistant Cells Independently of the P53 Gene
Lonidamine induces apoptosis in drug-resistant cells independently of the p53 gene. D Del Bufalo, … , A Sacchi, G Zupi J Clin Invest. 1996;98(5):1165-1173. https://doi.org/10.1172/JCI118900. Research Article Lonidamine, a dichlorinated derivative of indazole-3-carboxylic acid, was shown to play a significant role in reversing or overcoming multidrug resistance. Here, we show that exposure to 50 microg/ml of lonidamine induces apoptosis in adriamycin and nitrosourea-resistant cells (MCF-7 ADR(r) human breast cancer cell line, and LB9 glioblastoma multiform cell line), as demonstrated by sub-G1 peaks in DNA content histograms, condensation of nuclear chromatin, and internucleosomal DNA fragmentation. Moreover, we find that apoptosis is preceded by accumulation of the cells in the G0/G1 phase of the cell cycle. Interestingly, lonidamine fails to activate the apoptotic program in the corresponding sensitive parental cell lines (ADR-sensitive MCF-7 WT, and nitrosourea-sensitive LI cells) even after long exposure times. The evaluation of bcl-2 protein expression suggests that this different effect of lonidamine treatment in drug-resistant and -sensitive cell lines might not simply be due to dissimilar expression levels of bcl-2 protein. To determine whether the lonidamine-induced apoptosis is mediated by p53 protein, we used cells lacking endogenous p53 and overexpressing either wild-type p53 or dominant-negative p53 mutant. We find that apoptosis by lonidamine is independent of the p53 gene. Find the latest version: https://jci.me/118900/pdf -
Selective Estrogen Receptor Modulators for BPH: New Factors on the Ground
Prostate Cancer and Prostatic Disease (2013) 16, 226–232 & 2013 Macmillan Publishers Limited All rights reserved 1365-7852/13 www.nature.com/pcan REVIEW Selective estrogen receptor modulators for BPH: new factors on the ground M Garg1, D Dalela1, D Dalela1, A Goel1, M Kumar1, G Gupta2 and SN Sankhwar1 As the current management of BPH/lower urinary tract symptoms by traditionally involved pharmacological agents such as 5alpha- reductase inhibitors and a1-adrenoceptor antagonists is suboptimal, there is definite need of new therapeutic strategies. There is ample evidence in literature that suggests the role of estrogens in BPH development and management through the different tissue and cell-specific receptors. This article reviews the beneficial actions of selective estrogen receptor modulator (SERM) and ERb- selective ligands, which have been demonstrated through in vitro studies using human prostate cell lines and in vivo animal studies. SERMs have anti-proliferative, anti-inflammatory and pro-apoptotic mechanisms in BPH, and also act by inhibiting various growth factors, and thus represent a unique and novel approach in BPH management directed at estrogen receptors or estrogen metabolism. Prostate Cancer and Prostatic Disease (2013) 16, 226–232; doi:10.1038/pcan.2013.17; published online 18 June 2013 Keywords: selective estrogen receptors modulators; BPH; estradiol; estrogen receptor b INTRODUCTION relevant articles were selected for the discussion of role of SERMs in BPH in BPH is a common urological problem of aging males. It occurs in this review. about 10% of men below the age of 40 and increases to about 80% by 80 years of age.1 Clinical BPH is a benign enlargement of the prostate, which ESTROGENS AND ITS RECEPTORS: ROLE IN BPH results in voiding urinary difficulties that may, sometimes, Though BPH typically manifests in later stage of life when 2 significantly impair the quality of life in older patients. -
In the United States Court of Appeals for the Federal Circuit
Case: 18-1959 Document: 16 Page: 1 Filed: 08/20/2018 No. 18-1959 In the United States Court of Appeals for the Federal Circuit GENENTECH, INC., APPELLANT v. HOSPIRA, INC., APPELLEE ON APPEAL FROM THE UNITED STATES PATENT AND TRADEMARK OFFICE PATENT TRIAL AND APPEAL BOARD IN NO. IPR2016-01771 BRIEF OF APPELLANT GENENTECH, INC. PAUL B. GAFFNEY ADAM L. PERLMAN THOMAS S. FLETCHER WILLIAMS & CONNOLLY LLP 725 Twelfth Street, N.W. Washington, DC 20005 (202) 434-5000 Case: 18-1959 Document: 16 Page: 2 Filed: 08/20/2018 CERTIFICATE OF INTEREST Pursuant to Federal Circuit Rule 47.4, undersigned counsel for appellant certifies the following: 1. The full name of the party represented by me is Genentech, Inc. 2. The name of the real party in interest represented by me is the same. 3. Genentech, Inc. is a wholly-owned subsidiary of Roche Holdings Inc. Roche Holdings Inc.’s ultimate parent, Roche Holdings Ltd, is a publicly held Swiss corporation traded on the Swiss Stock Exchange. Upon information and belief, more than 10% of Roche Holdings Ltd’s voting shares are held either directly or indirectly by Novartis AG, a publicly held Swiss corporation. 4. The following attorneys appeared for Genentech, Inc. in proceedings below or are expected to appear in this Court and are not already listed on the docket for the current case: Teagan J. Gregory and Christopher A. Suarez of Williams & Connolly LLP, 725 Twelfth Street, N.W., Washington, D.C. 20005. 5. The title and number of any case known to counsel to be pending in this or any other court or agency that will directly affect or be directly affected by this court’s decision in this pending appeal are Genentech, Inc. -
Pdf; Chi 2015 DPP Air in Cars.Pdf; Dodson 2014 DPP Dust CA.Pdf; Kasper-Sonnenberg 2014 Phth Metabolites.Pdf; EU Cosmetics Regs 2009.Pdf
Bouge, Cathy (ECY) From: Nancy Uding <[email protected]> Sent: Friday, January 13, 2017 10:24 AM To: Steward, Kara (ECY) Cc: Erika Schreder Subject: Comments re. 2016 CSPA Rule Update - DPP Attachments: DPP 131-18-0 exposure.pdf; Chi 2015 DPP air in cars.pdf; Dodson 2014 DPP dust CA.pdf; Kasper-Sonnenberg 2014 phth metabolites.pdf; EU Cosmetics Regs 2009.pdf Please accept these comments from Toxic-Free Future concerning the exposure potential of DPP for consideration during the 2016 CSPA Rule update. Regards, Nancy Uding -- Nancy Uding Grants & Research Specialist Toxic-Free Future 206-632-1545 ext.123 http://toxicfreefuture.org 1 JES-00888; No of Pages 9 JOURNAL OF ENVIRONMENTAL SCIENCES XX (2016) XXX– XXX Available online at www.sciencedirect.com ScienceDirect www.elsevier.com/locate/jes Determination of 15 phthalate esters in air by gas-phase and particle-phase simultaneous sampling Chenchen Chi1, Meng Xia1, Chen Zhou1, Xueqing Wang1,2, Mili Weng1,3, Xueyou Shen1,4,⁎ 1. College of Environmental & Resource Sciences, Zhejiang University, Hangzhou 310058, China 2. Zhejiang National Radiation Environmental Technology Co., Ltd., Hangzhou 310011, China 3. School of Environmental and Resource Sciences, Zhejiang Agriculture and Forestry University, Hangzhou 310058, China 4. Zhejiang Provincial Key Laboratory of Organic Pollution Process and Control, Hangzhou 310058, China ARTICLE INFO ABSTRACT Article history: Based on previous research, the sampling and analysis methods for phthalate esters (PAEs) Received 24 December 2015 were improved by increasing the sampling flow of indoor air from 1 to 4 L/min, shortening the Revised 14 January 2016 sampling duration from 8 to 2 hr. -
Tanibirumab (CUI C3490677) Add to Cart
5/17/2018 NCI Metathesaurus Contains Exact Match Begins With Name Code Property Relationship Source ALL Advanced Search NCIm Version: 201706 Version 2.8 (using LexEVS 6.5) Home | NCIt Hierarchy | Sources | Help Suggest changes to this concept Tanibirumab (CUI C3490677) Add to Cart Table of Contents Terms & Properties Synonym Details Relationships By Source Terms & Properties Concept Unique Identifier (CUI): C3490677 NCI Thesaurus Code: C102877 (see NCI Thesaurus info) Semantic Type: Immunologic Factor Semantic Type: Amino Acid, Peptide, or Protein Semantic Type: Pharmacologic Substance NCIt Definition: A fully human monoclonal antibody targeting the vascular endothelial growth factor receptor 2 (VEGFR2), with potential antiangiogenic activity. Upon administration, tanibirumab specifically binds to VEGFR2, thereby preventing the binding of its ligand VEGF. This may result in the inhibition of tumor angiogenesis and a decrease in tumor nutrient supply. VEGFR2 is a pro-angiogenic growth factor receptor tyrosine kinase expressed by endothelial cells, while VEGF is overexpressed in many tumors and is correlated to tumor progression. PDQ Definition: A fully human monoclonal antibody targeting the vascular endothelial growth factor receptor 2 (VEGFR2), with potential antiangiogenic activity. Upon administration, tanibirumab specifically binds to VEGFR2, thereby preventing the binding of its ligand VEGF. This may result in the inhibition of tumor angiogenesis and a decrease in tumor nutrient supply. VEGFR2 is a pro-angiogenic growth factor receptor